Clinical and molecular pathological study of hippocampal scleroticdementia as mild cognitive impairment.

为了阐明海马痴呆的病理机制，我们研究了海马神经元的选择性丢失，这被认为不是缺血引起的。使用抗非磷酸化TDP-43多克隆抗体的免疫组织化学研究进行了与阿尔茨海默病的情况下，小脑浦肯野细胞保存完好，但海马CA 1区神经元消失，没有鬼缠结的海马。这表明神经元核TDP-43免疫染色的减少与神经元缠结和神经元细胞丢失无关。海马性痴呆的病理机制尚需进一步研究，海马性痴呆并非缺血性或惊厥性痴呆。

In order to clarify the pathomechanism of hippocampal dementia, we examined the selective loss of hippocampal neurons, which was not thought to be caused ischemia. Immunohistochemical study using anti-non-phosphorylated TDP-43 polyclonal antibodies was performed on the hippocampus in cases with Alzheimer's disease, in which cerebellar Purkinje cells were well preserved but hippocampal CA1 neurons were disappeared without ghost tangles. This indicated that decreased neuronal nuclear TDP-43 immunostaining had no relation with neurofibrillary tangles and neuronal cell loss. The pathological mechanism of hippocampal dementia, which was not suffering from ischemia and convulsion, should be examined more precisely.